RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
阻断 CXCR3B 表达增加肝细胞癌的肿瘤侵袭性
英文原题：Blocking CXCR3B Expression Increases Tumor Aggressiveness in Hepatocellular Carcinoma.
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Blocking CXCR3B Expression Increases Tumor Aggressiveness in Hepatocellular Carcinoma.
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研究概要
CXCR3B 可能通过减弱 NK 细胞对 HCC 的细胞毒性，在抑制 HCC 中发挥积极作用。
研究思路结论见上方概要
背景
CXCR3B 与抑制癌症和血管生成正相关。本研究探讨了 CXCR3B 在肝细胞癌细胞模型 SK-Hep1 中的作用。
方法
通过MTT法和流式细胞术检测了SK-Hep1中CXCR3B表达阻断对细胞活力、细胞周期和细胞凋亡的影响。此外，利用划痕迁移、transwell迁移和侵袭实验检测了阻断CXCR3B表达对细胞迁移和侵袭的影响。进一步，采用CytoTox96法分析了NK-92细胞对CXCR3B阻断的SK-Hep1的细胞毒性作用，并通过流式细胞术检测了与SK-Hep1共培养时NK-92细胞上NKp30+、NKG2D+和NKG2C+的表达。
结果
阻断CXCR3B表达对SK-Hep1细胞的活力、细胞周期或凋亡没有影响。然而，阻断CXCR3B表达显著增加了SK-Hep1的迁移和侵袭能力，同时增加了slug、vimentin和N-cadherin的蛋白表达。CXCR3B阻断降低了NK-92对SK-Hep1的细胞毒性，并抑制了NK-92细胞中活化受体NKp30+、NKG2D+和NKG2C+的表达。
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MATERIALS AND METHODS
The blockade of CXCR3B expression in SK-Hep1 was investigated in terms of cell viability, cell cycle, and cell apoptosis using MTT assay and flow cytometry. In addition, the effect of blocking CXCR3B expression on cell migration and invasion was examined using scratch motility, transwell migration, and invasion assays. Furthermore, the cytotoxic effect of NK-92 cells against CXCR3B blocked SK-Hep1 was analyzed using the CytoTox96 assay, and the expression of NKp30 + , NKG2D + , and NKG2C + on NK-92 cells in a co-culture with SK-Hep1 was measured using flow cytometry.
RESULTS
Blocking CXCR3B expression had no effect on the viability, cell cycle or apoptosis of SK-Hep1 cells. However, blockade of CXCR3B expression significantly increased the migratory and invasive ability of SK-Hep1 along with increased protein expression of slug, vimentin, and N-cadherin. CXCR3B blockade reduced the cytotoxicity of NK-92 against SK-Hep1 and inhibited the expression of activating receptors, NKp30 + , NKG2D + , and NKG2C + in NK-92 cells.
CONCLUSION
CXCR3B may play a positive role in suppressing HCC by attenuating natural killer cell cytotoxicity against HCC.
论文信息
- 作者
- Lee HH、Oh S、Kang H、Cho H
- 第一作者单位
- College of Pharmacy, Duksung Women's University, Seoul, Republic of Korea.South Korea
- 通讯作者单位
- College of Pharmacy, Duksung Women's University, Seoul, Republic of Korea; hyosun1102@duksung.ac.kr.South Korea
- 期刊
- Anticancer research2024 Dec
- 原文标识
- PubMed 39626933 · DOI 10.21873/anticanres.17357